TIDE Long Case PRO III Short Notes

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~ SHORT NOTES ~

by T.I.D.E team

Together in Delivering Excellence (T.I.D.E)

MEDICAL BASED SURGERY BASED

INDEX MEDICAL PAEDIATRIC PSYCHIATRIC SURGERY O&G ORTHOPAEDIC

2 30 53 59 80 108

“Ya Allah, Kuatkan Ingatan Kami Terhadap Apa Yang Kami Baca Ya Allah, Tutuplah Segala Kesalahan Jawapan Kami Semasa Dalam Peperiksaan Ya Allah, Berikanlah Ilham kpd Kami Untuk Menjawab Sepertimana Yang Pensyarah Kami Mahukan Ya Allah, Kurniakan Pensyarah Yang Baik Hati Dan Pemurah Sebagai Pemeriksa Kami Ya Allah, Kurniakanlah Pesakit Yang Baik Hati Dan Dapat Memberi Kerjasama Kepada Kami Nanti Ya Allah, Semoga Apa Yang Kami Baca Dan Paham Sahaja Yang Ditanya Dalam Peperiksaan Nanti” Aamiin….

Special appreciation to members of “T.I.D.E” Team

Copyright @ 2015 All Rights Reserved Final Year Medical Student (USM)

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Together in Delivering Excellence (T.I.D.E)

MEDICAL Notes

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Together in Delivering Excellence (T.I.D.E) Approach to Chest Pain [IQbaL] HISTORY 1.

2.

3. 4. 5.

Nature of chest pain ( SOCRATES )  Constricting (cardiac ischemic or oesophageal spasm)  Dull, central & crushing, last for 20min (MI)  Radiates to jaw & upper extremities (cardiac cause)  Sharp pleuritic pain that catch on inspiration (pleura or pericardium) & suggest pneumonia, pul. embolism or pericarditis  Sudden substernal tearing & radiate to back ( aortic dissection )

PHYSICAL EXAMINATION 1. 2. 3. 4. 5.

Abnormality of pulse rate and heart sound (cardiac) Crepitation – pneumonia or HF Reduced breath sound in one side – pneumothorax or lung collapsed Tenderness on chest – may causes from MSS however MI can present with chest tenderness GIT origin in normal cardiac and respi system

Pain brought on by food, lying down, hot drinks, or alcohol, and relieved by antacids – GIT causes (eg GERD, PUD, oesophaeal spasm) PMHx – known cardiac dz, HPT, HPL, smoking, FHx can support diagnosis Acute cholecyctitis & pancreatitis can cause pain referred to chest Associated Sx dyspnoea – cardiac ischemia, PE, pneumothorax or pneumonia

INVESTIGATION Basic Ix 1. 12 lead ECG unless non-cardiac causes is confidently being diagnosed eg pneumothorax  ST, QRS, arrhymias, tachy/brady  Pericarditis – widespread concave ST, PR depression 2.

CXR  can confirm respi disorder eg pneumothorax, pneumonia  can provide clues in cardiac dz (widened mediastinum in aortic dissection or a large globular heart in cardiac tamponade)

3.

Echocardiograhy

Laboratory a) Cardiac biomarker – CK-MB, Troponin I & T b) FBC – infection & screen for anaemia c) RFT – baseline d) TFT # some DDx can be excluded/confirmed after basic Hx, PE and these Ix – STEMI, pneumothorax, pneumonia, pericarditis

MANAGEMENT 1) 2)

Management will depends on diagnosis Psychological tx may be helpful in some pt

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Together in Delivering Excellence (T.I.D.E) Diagnostic Approach for Dyspnoea [IQbaL] Diagnostic Hypothesis COPD

Asthma

Pulmonary Etiologies Pulmonary embolism

Pneumonia (CAP, TB, Pneumocystic jiroveci pneumonia)

Intertitial lung disease (ILD)

Clinical Clues History  >20 pack years tobacco   Chronic cough +sputum   Progressive/persistent dyspnea  Exposure to occupational dust/chemical

Test

Treatment

 Spirometry (FEV1/FVC 100 mmHg

2.

Oxygenation

3.

Fluid challenge ( Hartmann’s solution )

4.

Diuretics

5.

Venodilators

6.

Inotropic agent

7.

Noradrenaline/adrenaline

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Together in Delivering Excellence (T.I.D.E) Details on Management 1. Oxygenation - Increase inspired oxygen to keep SPO2 more than 90% - Mechanical ventilation : if hypercapnia persist despite high flow oxygen (eg NIPPV) - Correct severe metabolic acidosis (pH less than 7.2 ) as it has negative inotropic and proarrthymogenic effect 2.

Fluid challenge ( Hartmann’s solution ) - If invasive hemodynamic monitoring is not available , fluid should be administered in small volumes (100ml ) over 510 min interval with reassessment of BP, heart rate, peripheral perfusion n breath sound. If BP does not responds to fluid (after 500-1000 ml), start vasopressor - If invasive hemodynamic monitoring is available, volume should be administered until a PCWP of 18 mmHg is attained

3.

Diuretics - IV frusemide 40 mg or bumetanide 1 mg at 20 min interval if initial therapeutic response is inadequate

4.

Venodilators - Sublingual nitroglycerin 0.3-0.5 mg up to 3 tabs every 5 min interval - IV nitroglycerin 5-10 microgram/min increased by 5-10 microgram/min every 5 -10 min - IV isoket ( isosorbide dinitrite) 2-10 mg/hr

5.

Inotropic agent - Dopamine 5-10 microgram/kg/min. low dose stimulates systemic vasodilation; high dose stimulates heart rate and contractility - Dobutamine 15-20 microgram/kg/min. acts at beta adrenergic receptor , no alpha adrenergic receptor activity

6.

Noradrenaline/adrenaline - Beta and alpha adrenergic agonist. Increase heart contractility and peripheral vasoconstriction - Noradrenaline : 8 -12 microgram/kg/min - Adrenaline : 0.05 – 0.1 microgram /kg/min

QUESTIONS 1. Medications ( MOA, dose and side effect ) 2.

Chest xray finding Cardiogenic pulmonary edema; cardiomegaly, widened mediastinum, bat wings, upper lobe diversion, kerley A,B,C, blunted costophrenic angle.

3.

PE finding for pulmonary edema

4.

Sign of right heat failure vs left heart failure

ECG findings ( ischaemic changes ST elevation, T inversion, Q wave ), duration and onset. Localization of infarction area. ( sbb associated dengan CAD )

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Together in Delivering Excellence (T.I.D.E) Rheumatic Heart Disease [Ain] HISTORY

PHYSICAL EXAMINATION

- RHD : A chronic heart condition caused by rheumatic fever that can be prevented and controlled. Rheumatic fever is caused by a preceding group A streptococcal (strep) infection. - Multisystem disease affecting connective tissue particularly of the heart, joints, brain, cutaneous and subcutaneous tissues 1. 2. 3. 4. 5. 6. 7. 8. 9.

Age ? - 5-15 yrs school-age children living in closed community (high risk group) Any history of fever or URTI preceeding to the complaint Any joint pain or others ass. symptoms eg.malaise,pallor,fatique ? Which joint affected,nature of the pain,is it migratory or localized? Any skin lesions or rash noted in the body? Any abnormal movement noted? Any swelling anywhere or nodule especially over bony prominence? Assess risk factor – overcrowding,poor sanitation, poverty,poor housing. Any complication symptoms eg.heart failure,atrial fibrillation

#The knees, ankles, elbows, and wrists are the joints most likely to become swollen from rheumatic fever. The pain often migrates from one joint to another.

INVESTIGATION 1. 2. 3. 4. 5.

FBC – anemia,leucocytosis Inflammatory marker – ESR/CRP positive Throats swab for group A streptococcus Anti-streptolysin O titre (ASOT) - elevated Investigations for evidence of carditis • Chest x-ray – cardiomegaly, pulmonary venous congestion • ECG- First degree A-V block, T wave changes, low voltage QRS • Echocardiogram – cardiac dilatation, valve involvement, pericardial effusion

Carditis in RHD : Mitral valve (90 %) : MR –children,adolescent MS – adult,later can get AF as cx. Aortic valve : AR,AS Less common affected : pulmonary, tricuspid MANAGEMENT Principle of management : -

Step I - primary prevention (eradication of streptococci) Step II - anti inflammatory treatment (aspirin,steroids) Step III- supportive management & management of complications Step IV- secondary prevention (prevention of recurrent attacks) Step v – tertiary prevention

1. Bed rest until CRP normal for 2 weeks (maybe by 3 months) 2. Benzylpenicillin 0.6-1.2g IM or Penicillin V 250-500 mg 2-3 times daily for 10 days. (if allergic give erythromycin or azithromycin for 10 days) 3. Analgesia for carditis/arthritis :aspirin 100 mg/kg/d in divided dose (max 8g/d) for 2 day then 70 mg/kg/d for 6 weeks.  if moderate to severe carditis : add prednisolone 4. Immobilize joint in severe arthritis – rest and supportive splinting 5. Treatment of chorea - Haloperidol (0.5 mg/8h) or diazepam 6. Secondary Prevention of Rheumatic Fever- aims to prevent illness or progression of disease once a problem has been identified  Benzathine penicillin G 1 200 000 U every 3 weeks* Intramuscular  Penicillin V 250 mg twice daily Oral # For individuals allergic to penicillin : Erythromycin 250 mg twice daily 7. Tertiary prevention–aims to prevent complications once a disease is established. Reducing symptoms to minimise disability and prevent premature death. Eg.heart valve surgery, medication to manage heart failure eg.diuretics and preventing stroke.

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Together in Delivering Excellence (T.I.D.E) 1. Diagnosis of RHD JONES criteria : evidence of recent strep infection plus 2 major criteria or 1 major criteria + 2 minor

# Exceptions to Jones Criteria -

Chorea alone, if other causes have been excluded Insidious or late-onset carditis with no other explanation Patients with documented RHD or prior rheumatic fever,one major criterion,or of fever,arthralgia or high CRP suggests recurrence

2. Duration of Secondary Rheumatic Fever Prophylaxis    

Fever without carditis - At least 5 y or until age 18 y Rheumatic fever with carditis and heart disease (persistent valval lesion) - At least 10 y since last residual episode and at least until age 40 y,sometimes lifelong prophylaxis Rheumatic fever with carditis & heart disease (no valvar lesion) -10 y or well into adulthood More severe valvular disease,post-valve surgery cases - lifelong

3. Differential diagnosis of acute rheumatic fever based on symptoms

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Together in Delivering Excellence (T.I.D.E) COPD [Rozana] HISTORY

PHYSICAL EXAMINATION

Epidemiology : > 35 yo, 10-20% in over 40s

General : Tachypnoea, use of accessory muscle, wheeze, cyanosis

Chronic bronchitis : defined clinically as cough, sputum production, on most days for 3 months of 2 sucessive years, sx improvise if pt stop smoking

Specific :  sign of airflow limitation and air trapping in advanced stage (barrel chest, loss of cardiac and liver dullness, prolonged expiration, reduced breath soundhyperinflation, reduce expansion)

Emphysema : define histologically as enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls

Cx : cor pulmonale: edema, ↑ JVP, pneumothorax Risk factor : Genes (alpha-1 antitrypsin enzyme deficiency causes panlobular emphysema), Exposure to particles, Tobacco smoke, Organic and inorganic occupational dusts, Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings, Outdoor air pollution, Lung growth and development, Oxidative stress, Respiratory infections, Socioeconomic status Sx :  

chronic cough, sputum, dyspnoea(interfere daily activities), wheeze, chest tightness extrapulmonary : LOW, cor pulmonale sx

Complication : acute infection +/- infection, polychythaemia, respi failure, cor pulmonale, pneumothorax, lung carcinoma, osteoporosis INVESTIGATION Laboratory : FBC =anemia of chronic disease, PCV ↑(chronic hypoxemia) Others :  Spirometry : post bronchodilator FEV1/FVC ratio < 0.7 = not fully reversible airflow limitation

MANAGEMENT Mx of acute COPD  Controlled oxygen therapy  Nebulized bronchodilators (salbutamol and ipratropium)  Steroids (IV hydrocortisone and oral prednisolone)  Antibiotics, if evidence of infection  Physiotherapy to aid sputum expectoration  If no response  repeat nebulizers and consider iv aminophlline  If no respone 1) Consider nasal intermittent positive pressure ventilation. 2) Consider intubation & ventilation Mx of stable COPD Non pharmaco/ general : smoking cessation, encourage exercise, treat poor nutrition or obesity, influenza and pneumococcal vaccination Pharmaco  Mild (FEV1 50-80% predicted) : antimuscarinic eg. Ipratropium/ B2 agonist inhaled PRN



Peak expiratory flow rate : low





ECG :detect pulmonary HPT ( advanced disease) right atrial and ventricular hypertrophy (cor pulmonale) ABG : PaO2 ↓+/- hypercapnia

Moderate (FEV1 300-49% predicted) : regular anticholinergic eg. Ipratropium or long acting inhaled B2 agonist eg. salmeterol + inhaled corticosteroid eg. beclamethasone



Severe (FEV1 ) : LABA + inhaled steroid, anticholinergic.



Imaging :  Hyperinflation (flattened diaphragm and increased lung volume), large central pulmonary arteries, ↓ peripheral vascular marking, bullae, hyperlucency of lung  Exclude other diagnosis eg. Lung cancer, heart failure, bronchiectasis and TB

Pulmonary HPT : Assess the need of LTOT(long term 02 therapy), treat edema with diuretics

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Together in Delivering Excellence (T.I.D.E)

Pink puffers & blue bloaters (end of a spectrum)  

Pink puffers have ↑ alveolar ventilation, a near normal PAO2 and normal or low PCO2, breathless but not cyanosed, may progressed to type 1 respi failure Blue bloaters have ↓ alveolar ventilation, with low PAO2 and high PACO2, cyanosed but not breathless and may go on to dev. Cor pulmonale

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Together in Delivering Excellence (T.I.D.E) Tuberculosis [Fatin] HISTORY o

o

o

o

Epidemiology  Mycobacterium tuberculosis  Transmit through microscopic droplet ( cough, sneeze, speaking) Risk factor  Immunocompromise (DM, chronic dz, HIV, steroid, malnutrition)  Travelling to endemic area  Substance abuse (drug/alcohol)  Contact with TB pt (occupation, family member)  Living in overcrowded area  Prev TB infection S&S  Chronic cough >2w  Blood stained cough  LOW, LOA  Fever, night sweat  SOB, chest pain, pleuritic chest pain  Extra-pulmonary : hematuria (renal), back pain (spine), seizure (meninges) Complication (lymphatohematogenous spread)  Extra-pulmonary TB -bone, brain, liver&kidney, heart  ARDS  Lung failure  Relapse of disease

PHYSICAL EXAMINATION o

General  Cachexic  Fever  Muscle wasting

o

Specific  Lung :  Consolidation =↓chest expansion, dull percussion, bronchial BS, crepitation  Pleura effusion = trachea deviated if massive, ↓chest expansion, stony dull, absent BS, ↓vocal resonance  Lung collapse = trachea deviation ipsilateral mediasternal shift, ↓chest expansion, dull, absent/reduce BS  Other : lymphadenopathy

∆∆ 1) pneumonia 2) lung carcinoma 3) lung abscess 4) fungal infection

INVESTIGATION o

o

Laboratory  FBC –leucocytosis as sign of infection or anaemia due to chronic disease  Sputum direct smear for AFB  Mantoux test- result read after 72H  Sputum c+ sensitivity –3 morning specimen  Sputum cytology- to look for any abnormal cells to suggest malignancy  Blood culture + sensitivity :to detect any microorganism  Broncoscopy - tumour, foreign body, inflammation  Pleura fluid analysis (pleura tapping) Imaging  X-ray :  Primary TB: perihilar and paratracheal lymphadenopathy, patchy area of consolidation, pleura effusion feature  Post 1® TB: consolidation at post segment of upper lobe @ sup segment of lower lobe, tuberculoma at Rt upper lobe, cavitation  Milliary TB : millet seed nodule (1-3mm) evenly distributed

MANAGEMENT Anti-TB therapy  Intensive phase (2M) -> 2EHRZ  Maintainence phase (4M) -> 4HR ST

1 LINE : Rifampicin (R)-hepatitis Isoniazid (H)- hepatitis Pyrazinamide (Z) –joint and ms pain Ethambutol (E)- visual disturbance Streptomycin (S) – ototoxicity DOTS –directly observed therapy short case

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1)

Screening of high risk group  HIV pt  Immigrant  Person in prison/drug rehab centre  Pt with dm, renal dz, steroid, immune sup drug  Hemato malignancy

2)

Classification of TB  PTB +ve smear : * 2 sputum smear positive AFB * 1 sputum +ve AFB and +ve radiological finding * 1 sputum +ve AFB and +ve culture 

3)

PTB –ve smear : * 3 sputum smear –ve * sputum smear –ve but subsequent culture +ve

TB meningitis Tx   

The duration of anti –tb is longer which for 12 months duration Intensive(2 months) maintenance (10 months) Other drug to give is steroid (6 weeks or longer)

4) Preventive measures Primary intervention  Identification + immediate isolation  Herd immunity-BCG vaccination  Contact tracing of individual who are in close contact with cases  Reduce risk of transmission by using ppe(personal protective equipment), cough etiquette 5)

Why hemoptysis occur? Due to erosion of vessel located in the wall of cavity or rupture of dilated vessel in cavity

6)

Mantoux test

7) Follow up : every 2 months, take CXR and sputum smear AFB 8) Intensive therapy 2 months, then maintenance therapy 4 months but can be extended when : Cavitating lesion in CXR Extrapulmonary TB Immunocompromised pt

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Together in Delivering Excellence (T.I.D.E) Lung Cancer ( Bronchogenic Carcinoma) [Zuraidah] HISTORY

Def : malignancy of the lung arising from the epithelium of the bronchial tree. nd

Prevalence : 2 after prostate ca in men , breast ca in women. Aetiology : smoking, asbestos exposure, radon gas exposure, familial predisposition (genetic), HIV infection, air pollution (pesticide), lung diseases. History : 0 1. Sx related to 1 tumor: cough, dyspnea, hemoptysis, chest pain, postobstructive pneumonia 2.

Sx related to mediastinal spread: - Hoarness of voice with left sided lesion (caused by recurrent laryngeal nerve palsy - Obstructive of svc with right sided tumor or asso lymphadenopathy - Elevation of hemidiaphragm from phrenic nerve palsy - Dysphagia from esophageal obs and pericardial temponade

PHYSICAL EXAMINATION

General - Hoarseness of voice, Cachexic, alopecia (chemo), nicotine staining, cyanosis, clubbing, flaps, cervical l/n, raised JVP + sign of SVC obstruction, leg edema - Vital sign – tachypnea * Horner syndrome (ptosis), paraneoplastic synd ( wasting of small ms of hand) Specific (Respiratory system) Inspection Barrel shaped, mvmnt of chest reduce on affected, use of accessory ms Palpation Trachea deviation, apex beat, chest wall tenderness (mets), inc tactile fremitus Percussion - dullness, liver span enlarged (mets) Auscultate - bronchial bs, rhonchi, rub DDx

3.

Sx related to mets: sites liver, brain, pleural cavity, bone, adrenal glands, contralateral lung & skin

4.

Paraneoplastic synd: - Pain in arm/legs caused by hypertrophic osteoarthropathy - Sx of hypercalcemia caused by scc

5.

Systemic effects: fever, anorexia, low/loa, weakness, profound fatigue INVESTIGATION

Laboratory FBC: WBC raised in concomitant infection ABG: hypoxia with respi acidosis in severe endobronchial obs ESR: > 100 in 1hour Serum sodium, calcium Sputum examination – malignant cell cytology, c+s for any u/l lung infection Lung fx test: FEV1 of 1000ml after planned resection Invasive: pleural fluid cytology, percutaneous transthoracic needle biopsy

Imaging - CXR: 0  1 tumor - hilar mass or coin lesion, rib erosions, raised hemidiaphragm (phrenic nerve palsy), lymphangitis carcinomatosis, any lung collapse 0  if 2 tumor – cannon ball appearance - CT scan TAP: metastasis, staging - Bronchoscopy (+washing & brushing): endobronchial tumor - Bone scan: staging

1. 2. 3. 4. 5.

Pulmonary TB Pneumonia Lung abscess Bronchiectasis Sarcoidosis

MANAGEMENT

Depends on multiplicity factors: 0 It is a 1 or mets lesion Hilar or mediastinal infiltration Chest wall involvement Asso with complication- massive pleural effusion, svc obstruction, collapse-consolidation Phrenic nerve involvement Paraneoplastic syndromes Treatment : 1) Surgery Lobectomy- the most effective type of surgery, even when the lung tumor is very small. A wedge- remove the tumor, surrounded by a margin of normal lung. Segmentectomy- removes the portion of the lung where the cancer developed. Pneumonectomy. If the tumor is close to the center of the chest, remove the entire lung. Radiofrequency ablation- needle inserted into the tumor to destroy the cancer with an electrical current * SCLC is not recommended for surgery d/t aggressive & micromets. Go for chemo 2) Medical – chemotherapy or radiotherapy 3) Treatment for sx such as infection & breasthless 4) Pain management & quality of life 5) Adequate hydration & food intake

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer

1. Cx of lung ca? i. Hemoptysis ii. Acute breathlessness d/t endobronchial narrowing iii. Massive, recurrent hemorrhagic pleural effusin iv. SVC obstruction v. Paraneoplastic syndrome

3. Contraindication for surgery? i. Metastatic carcinoma ii. FEV1 < 15000ml iii. Severe pulmonary hpt iv. Uncontrolled major cardiac arrhythmias v. Co2 retention vi. Myocardial infarction in the past 3 months

2. Aim of staging? To identify candidates for surgical resection, since this approach offers highest potential cure

4. Which tumor respond well to chemo? Small cell lung ca (SCLC), combination of cisplatin & etoposide is the best therapeutic index of ay regime Role for chemo in non small cell ca (NSCLC) suggested that bnefits are small

Notes Types : Small cell lung ca (SCLC) – 20%, rapid growing, strong correlation with smoking, mets rapidly to various organ (liver, brain, bone, git, adrenal glands ), histologically- keratinization Non small cell lung ca (NSCLC) – 80% I. Adenocarcinoma (50%), commonly seen in non smoker, arises from bronchial mucosal glands in the outer, or peripheral area of lungs, histo-gland formation II. Squamous cell carcinomas (30%), aka epidermoid carcinomas, centrally located, cavitary lesion, histo- presence of keratin pearls and has tendency to exfoliate. III. Large cell carcinomas (20%), undifferentiated ca, large peripheral mass on cxr, histo-highly atypical cell with focal necrosis Anatomical Staging -

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Together in Delivering Excellence (T.I.D.E) Bronchiectasis [Rafidah] HISTORY Definition: Abnormal and permanent dilated airways resulting from Inflamed thickened and irreversibly damage bronchial walls cause mucociliary transport mechanism become impaired and frequent bacterial infection ensues.

Aetiology: 

 

Congenital: cystic fibrosis, Primary ciliary dyskinesia, Kartagener’s syndrome Post-infection: measles, pertussis, Bronchiolitis, pneumonia, HIV, TB Bronchial obstruction: tumour, foreign body Rheumatoid arthritis, IBD Allergic bronchopulmonary aspergillosis

     

Cough with copious purulent sputum Recurrent hemoptysis SOB Intermittent fever and night sweat History of recurrent infection Weight loss



 

PHYSICAL EXAMINATION General: Respiratory distress Finger clubbing Specific: Coarse crackles over affected area, usually basal lung Sign of collapse, fibrosis or pneumonia

S&S

Complication      

Pneumonia Pleural effusion Pneumothorax Hemoptysis Cerebral abscess amyloidosis INVESTIGATION

Laboratory Full blood count – white cell count (infection) Sputum culture Imaging Chest radiograph: cystic shadow, thickened bronchial walls(tramline and ring shadow) High resolution CT scan – thickened, dilated bronchi and cyst at the end bronchioles. Bronchoscopy – to locate site of hemoptysis or exclude obstruction

MANAGEMENT Non surgical: Non pharmacological 1) Postural drainage at least 3 times daily for 10 – 20min Pharmacological 1) Antibiotic: according bacterial sensitivities 2)

Bronchodilator: may be useful in asthma, copd,cf, allergic bronchopulmonary aspergillosis

3)

Corticosteroid: eg. prednisolone

Surgical : resection of the affected lobe

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1)

What are the major respiratory pathogens in bronchiectasis? Staph. Aureus, pseudomonas aeruginosa, H. influenza, and anerobes

2)

What are the common site for localized disease? Left lower lobe and lingula

3)

What is the indication of surgery in bronchiectasis? Bronchiectasis localized to a single lobe or a segment without clinical, bronchographic, ct evidence of bronchiectasis of bronchitis affecting other parts of the lungs.

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Together in Delivering Excellence (T.I.D.E) Pleural Effusion [Farhan] HISTORY

PHYSICAL EXAMINATION

 Accumulation of fluids in the pleural space  Transudates (35g/L):  Increased leakiness of pleural capillaries due to  Infection (pneumonia, tuberculosis)  Ischemia (pulmonary infarction, SLE, rheumatoid arthritis)  Malignancy (bronchogenic ca, malignant mets, lymphoma)

 Chest examination (only apparent if effusion > 300ml):  Inspection: asymmetrical chest movement  Palpation: reduced chest expansion, mediastinal shift, trachea deviation (>1000ml), decreased tactile fremitus,  Percussion: stony dullness  Auscultation: Reduced or absent breath sound, reduced vocal resonance

 Common complaints: dyspnea, cough, pleuritic chest pain.  Ask about associated symptoms e.g. dyspnea with bilateral leg swelling, orthopnea, and PND  CCF; or night sweats, fever, and weight loss  TB  Ask about occupation; might give a clue to illness

INVESTIGATION  CXR (PA):  Blunted costophrenic angle (small effusion)  Clear air fluid level with concave upper border  Air fluid level with flat upper border (presence of pneumothorax)  Lateral decubitus film is useful to detect smaller effusion; layering of an effusion indicates free flowing effusion  Pleural fluid analysis (send for):  Clinical chemistry (protein, glucose, pH, LDH, amylase)  Bacteriology (microscopy & culture, TB culture)  Cytology  Immunology (RF, ANA, complement) – if indicated  Pleural biopsy  If pleural fluid analysis is inconclusive

MANAGEMENT  Transudative effusions are managed by treating underlying causes  If effusion is symptomatic (exudative/transudative) drainage can be done to provide relief  Drain fluid slowly (max 2L/24h)  If drain large amount quickly; it can cause re-expansion pulmonary edema  Pleurodesis (pleural sclerosis)  Talc, tetracycline, bleomycin sulfate, zinc sulfate  Thoracoscopic talc pleurodesis most effective for malignant effusions  S/E: fever, chest pain, nausea  Surgery  Persistent collections and increasing pleural thickness (on ultrasound) requires surgery – pleurectomy

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Light’s criteria To differentiate between transudate and exudate for proteins ranged in between 25 – 35g/L According to Light’s criteria, the fluid is exudate if:  Effusion protein : serum protein ratio > 0.5  Effusion LDH : serum LDH ratio >0.6  Effusion LDH level is greater than 2/3 of the upper limit of serum LDH

Pleural fluid analysis Normal pleural fluid characteristics  Clear ultrafiltrate of plasma that originates from the parietal pleura  A pH of 7.60-7.64  Protein content of less than 2% (1-2 g/dL)  Fewer than 1000 white blood cells (WBCs) per cubic millimeter  Glucose content similar to that of plasma  Lactate dehydrogenase (LDH) less than 50% of plasma Sample Clear, straw-coloured Turbid, yellow Haemorrhagic Clinical chemistry Glucose 3 Months) [Khiru] HISTORY In history: i) Past UTI ii) known BP, DM, FHx iii) Drug hx (NSAIDS, gentamycin, sulphonamides, tetracyclines, vancomycin,amphotericin, cisplatin, ACEi, ARB, methotrexate, heavy metal poisoning) iv) Fatigue, weakness v) Anorexia, vomiting, metallic taste vi) Pruritus vii) Bone pain viii) Dyspnea ix) Ankle swelling Causes        

PHYSICAL EXAMINATION Signs: pallor, yellow skin pigmentation, brown nails, purpura, bruising, excoriation, increase BP,cardiomegaly, pericardial rub, peural effusion, pulmonary or peripheral edema, proximal myopathy

Acute kidney injury DM HPT Glomerulonephritis/ pyelonephritis Polycystic kidney disease Renal vascular disease Analgesic nephropathy (antipyretics, caffeine, NSAIDs) Med

Complication  Electrolyte: hyperk,hypoCa,hyperphosphatemia  Haematological: anemia, bleeding tendency (plt dysfunction)  CVS: cardiac failure, HPT, pericarditis, accelerated atherosclerosis  Neurological: drowsy, seizure, peripheral neuropathy  Metabolic/ endocrine: hyperlipid, renal osteodystrophy  GIT: anorexia, N&V, bleeding  Skin: pruritus, easy bruising

INVESTIGATION 1. Blood: Hb reduced (normochromic normocystic), ESR, Urea & electrolyte (increase urea & creatinine), glucose (DM), reduced calcium, increase phosphate, increase alkaline phosphate (renal osteodystrophy), increase PTH 2. Urine: microscopic culture & sensitivity, dipstick, 24H urinary protein

3. Imaging: renal ultrasound-renal size small, indirect normal 3:7), raised ALP II. gamma-glutamyltransferase-if dx ambiguous. I.

Benign  Recurrent spikes of similar jaundice that resolves on their own times (suggest obstruction : stones,stricture)  Young pt with painful jaundice  Previous hx of gallstone/biliary colic sx  Previous biliary surgery/ibd (sclerosing cholangitis)

Malignancy  Old pt, new onset of jaundice & progressively worsening  No associated pain  Constitutional sx  Mets sx (bone pain, neck lump, dyspnea)  Late pain, constant & relentless (pancreatic ca)

4.Complication  Sx of cholangitis (fever,chills,rigor,RHC pain,jaundice)  Pruritus  Pancreatitis(gallstone as a cause)  Decompesation (heapatic encephalopathy,fetor hepaticus, worsening ascites)  Fat malabsorption (steatorrhea,fat soluble vit deficiency ADEK-coagulopathy.

2.

To confirm inflammation/infection I. FBC: Hb, WBC II. Renal profile : electrolyte(nutritional status), U:C ratio III. Coagulation profile prolong PT (vit k malabsorption, liver dysfx) IV. Tumor marker : CA 19-9, CEA (cholangioca&pancreatic ca) V. Blood C&S : TRO HBS sepsis (if fever&febrile) VI. GXM : in case op

3. I.

Imaging HBS US  choledolithiasis - duct dilate>8cm  Gallstone dis/cholecystitis - GB stone/sludge, thickned GB wall, pericholecystic fluid, fat stranding  cx gall stone  liver consistency (fatty/cirrhotic)

II. III.

CTAP : if suspect perforated,TRO ca CXR : ARDS in cholangitis,p.effusion



MANAGEMENT According to cause

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer Notes [any classification,staging, mnemonic etc] 1.

Define jaundice:  Yellowish discoloration of kin, sclera and mucus membrane d/t bilirubin, a yellowish pigment  Usually clinically evident when serum bilirubin >3mg/dl (51.3umol/L)  Normal bilirubin: 3-17 umol/L

2.

Bilirubin transport

3.

Causes  Painless: CA,HOP,cholangioca,Periam ca  painful: Stricture,hepatic causes

Intraluminal Benign 1.Gallstone 2.Parasitic infection (schistosomiasis)

Mural Benign 1. Stricture (post instrumentation & post inflammation) 2. Primary sclerosing cholangitis 3. Choledochal cyst Malignant 1. Cholangiocarcinoma

Extramural Benign 1. Mirizzi syndrome 2. Pancreatitis Malignant 1. Head of pancreas ca 2. Periampullary ca 3. Mets to porta hepatis

4.

What is Corvoisier’s Law  If the gallbladder is enlarged& patient is jaundiced, the cause is unlikely to be gallstone

5.

Whait is Charcot’s triad  triad of fever, RHC pain &jaundice : suggest cholangitis.

6.

Urine & blood biochemistry in jaundice - Liver enzyme in ix of jaundice  ALP (alkaline phosphatase) & GGT : markers of cholestatis  ALT (alanine aminotransferase) & AST (aspartate aminotransferase) : markers of hepatocellular injury  AST: ALT ratio>1 → alcoholic hepatitis (remember ST out)

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Together in Delivering Excellence (T.I.D.E) Multi-nodular Goitre (MNG) [Alliah] HISTORY 

Definition  Enlarged and diffusely heterogenous thyroid gland



Epidemiology  6x more common in woman



Check list hx for MNG :  Establish details of the swellingonset,duration,progression,recent growth,pain  Other neck symptoms(local) - discomfort during swallowing, SOB,pain and hoarseness of voice  General sx - sx of endocrine dysfunction  Past medical hx - hx of radiation to the neck during childhood  Family hx of autoimmune disease



DDx  Anaplastic carcinoma of thyroid  Autoimmune thyroiditis

PHYSICAL EXAMINATION General  Moderate body built. Neither nervousness nor lethargic  Skin - normal (no sweating;not dry)  Hair - normal  Hands – no wasting or puffiness  Normal PR with no fine tremor  No eye signs  There may be general signs of thyrotoxicosis or in elderly pt with very long-standing nodular goitres, the signs of myxoedema. Specific  A nodular swelling in front of the neck which moves upwards on swallowing  Non – tender  Smooth surface but assymetrical nodular  Firm in consistency  Neither skin or nerby muscle attachment  No signs of airway obstruction  Cervical LN not palpable  No bruits over the gland

INVESTIGATION Laboratory 1)

2)

3)

TFT  To exclude mild hyperthyroidism  TSH : normal (0.5-5mu/L)  Free T4 : normal (9-24)  Free T3 : normal (2.2-5.4) Thyroid antibodies  To exclude autoimmune thyroiditis  Thyroid peroxidase (TPO) antibody – up to 25units/ml  Anti-thyroglobulin titres : significant when > 1:100 titres FNAC  Will only be required for dominant swelling in a generalised goitre

Imaging 1) 2)

Plain radiographs of chest and thoracic inlet  To exclude tracheal deviation or compression U/S and CT scan

MANAGEMENT Pharmaco  Thyroxine Surgical  Total thyroidectomy and lifelong replacement of thyroxine  Conventional subtotal thyroidectomy – leave up to 8g of relatively normal tissue in each remnant

72

Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1.

Classification of thyroid swelling Simple goitre (euthyroid)  Diffuse hyperplastic (physiological,puberty,pregnancy)  MNG

Toxic  Diffuse (Grave’s Dz)  Multinodular  Toxic adenoma

Neoplastic (Benign & Malignant)  Inflammatory  Autoimmune (Hashimoto’s dz)  Granulomatous (De Quarvain’s thyroiditis)  Fibrosing (Riedel’s thyroiditis)  Infective (acute and chronic)  Other - amyloid

2.

Complication 1) Tracheal obstruction  Due to gross lateral displacement or compression in lateral or AP plane by retrosternal extension of goitre 2) Secondary thyroitoxicosis (up to 30% pt)  Transient episodes of mild hyperthyroidism 3) Carcinoma (incidence 5-10%)

3.

Indication for surgery  Cannot be treated medically – failed or unsuitable for medical tx  Cancer  Compression on neighbouring structures  Cosmetic  Compliance/cost problems – with long term medical therapy

4.

Postoperative complication after thyroidectomy (mostly H’s, One I’s, One T’s)

   

IMMEDIATE (< 24hrs) Haemorrhage with hematoma formation Hoarness or airway compression Hyperthyroidism Tracheomalacia

 

EARLY (< 1m) Infection Hypoparathyroidism leading to hypocalcemia

   

LATE (> 1m) Hypothyroidism Hyperthyroidism Permanent hypoparathyroidism Hypertrophic scarring or keloid formation

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Together in Delivering Excellence (T.I.D.E) Hematuria [Ain] HISTORY

PHYSICAL EXAMINATION

Definition : >3 rbc/hpf  DDX     1.

2.

Haemoglobinuria Myoglobinuria pseudohematuria(menses) meds causing discolouration (rifampicin,phenytoin)

Which part of urine stream is blood stained?  Initial phase-bleeding from urethra distal to urogenital diaphragm  Throughout urination – upper urinary tract or upper bladder  End of urine stream- bladder neck or prostatic urethra

Painful hematuria

Painless hematuria

UTI Pyelonephritis Hydronephrosis Renal cysts Ureteric stone BPH,strictures tumour

Malignancy- RCC, bladder,prostate Drugs Glomerulonephritis ITP/HSP Bleeding diathesis Infection-malaria,schistosomiasis Exercise-joggers hematuria

Severity – any clots,s/s of anemia Ass. symptoms –frequency, dysuria, LUTS symptom, fever  DDX : nephrolithiasis, pyelonephritis, UTI, malignancy, bladder outflow obstruction. 5. Others – drug hx, malignancy symptom, recent travelling, sore throat, medical illness eg: coagulopathy, autoimmune ds INVESTIGATION

 



  

Is it painful or painless?

3. 4.



 

Urine – dipstick, UFEME ,urine cytology for malignant cells, urine phase contrast, urine C&S Blood – FBC,BUSE,PT/APTT,GXM Imaging : Upper tract - imaging, lower tract - cystoscopy Plain KUB : stone, size of kidney Ultrasounds of kidney :renal size, stones, hydronephrosis, hydroureters Intravenous urogram (IVU) – C/I in contrast allergy, renal impairment (cr>200),on metformin cause lactic acidosis, asthma given steroids 3 days b4 study, pregnancy CT Urogram/IVP Cystoscopy : detection of bladder tumour, biopsy can be taken at the same time Kidney biopsy –suspect glomerular disease

  

Vital sign: hypotension and tachycardia are seen in patients who are haemodynamically unstable from acute blood loss,high temperature in infection Sign of anemia – pallor of conjunctiva, skin Periorbital, scrotal, and peripheral oedema: may indicate hypoalbuminaemia from glomerular or renal disease. Cachexia: may indicate malignancy. Abdomen- renal/bladder mass, palpable bladder (AUR),flank tenderness, suprapubic tenderness Scrotum – varicocele on the left (RCC of left kidney with extension of tumour to renal vein, block testicular vein from drained to left renal vein) External genitalia - blood from urethra, trauma, laceration Digital rectal examination – prostate enlargement ( BPH vs cancer) The presence of a urethral catheter, suprapubic catheter, ureteral stent, or nephrostomy tube may signify an iatrogenic cause of bleeding that is generally benign

MANAGEMENT Depends on disease  Asymptomatic (isolated) hematuria generally does not require treatment. In conditions associated with abnormal clinical, laboratory, or imaging studies, treatment may be necessary, as appropriate, with the primary diagnosis.  Surgical intervention may be necessary in certain anatomical abnormalities, such as ureteropelvic junction obstruction, tumor, or significant urolithiasis.  Consultations are required in patients with urinary tract anomalies and in some patients with systemic diseases (eg, bleeding disorders, collagen vascular diseases, sickle cell nephropathy).  Referral to a urologist is required when clinical evaluation and workup indicates a tumor, a structural urogenital abnormality, or an obstructing calculus.

74

Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer

Urine dipstick Positive for hematuria

No blood cell

urine microanalysis

blood cell present If no proteinuria (isolated hematuria) -need to ix for systemic ds Coagulation studies,complete blood count,hb electrophoresis

Myoglobinuria or hemoglobinuria

If proteinuria-suspect glomerular ds and require kidney biopsy

If pyuria and bacteriuria –obtained urine culture (if –ve,consider interstitial nephritis)

Causes of hematuria : Pre-renal

• • • •

Renal

• • •

Post-renal

• • •

Drugs: analgesics(NSAIDS), anticoagulants, CPM, OCP Systemic : sickle cell diasease, haemophilia, ITP Metabolic: hypercalciurea, DM Vascular: AV malformations, renal artery ds,renal vein thrombosis Glomerular: post-strep AGN, IgA nephropathy, lupus nephritis Interstitial: polycystic kidney disease, stone, malignancy Vascular: HSP, Wagener granulomatosis Infections of ureter, bladder, prostate, urethra Cancer of ureter, bladder, prostate, urethra Stone

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Together in Delivering Excellence (T.I.D.E) Prostate Cancer [Fatin] HISTORY o

o

o

o

Epidemiology : th  4 most common cancer among men  Peak age : 65-75 y.o Risk factor :  Age  Obesity  FHx  A/w ↑BP S&S :  Asymptomatic – incidental finding on DRE  Obst LUTS (hesitancy, staining on urinate, weak stream, prolonged micturition, terminal dribbling, incomplete voiding)  Cx LUTS – hematuria, infection, stone, obst uropathy @renal failure  IPSS (incomplete voiding, frequency, intermittency, urgency, weak stream, straining, nocturia) Complication :  Metastatic sx – lower back pain (from Batson venous plexus)  Other place: LN, rectum, bladder, lower ureter

PHYSICAL EXAMINATION

o

o

o

INVESTIGATION o

Diagnosis :  Transrectal ultrasound (TRUS) with core biopsy (2 specimen) -histology GLEASON score – degree of differentiation/microscopic appearance  PSA level 50 g  post ejaculation  urethral injury  UTI  iatrogenic (flexible scope)

4.

Source of testosterone  testes  adrenal gland  fat

5.

Family history of – BRCA1, BRCA2, HPC1

6.

Pre-op assmnt of TRUS w biopsy  take consent  bowel prep –ducalex/ravin supp 3 days b4 procedure  analgesic – on table b4 procedure (lignocaine)  antibiotic – 3 days b4, 2 days after - quinolone –penetrate prostate -metronidazole  after TRUS – no ridding - no heavy lifting - no SI

7.

Function of prostate  secretes an alkaline fluid at the time of ejaculation.  alkaline fluid helps neutralize the acidic environment of the female vaginal tract, prolonging the lifespan of sperm and providing better motility

8.

What is PSA (prostate specific antigen)?  protein / tumor marker produced by epithelial cells of the prostate gland

77

Together in Delivering Excellence (T.I.D.E) Renal Calculi [Dalilah] HISTORY 1.

RENAL STONES Asymptomatic unless stone gets lodge in the pelviureteric junction May cause hydronephrosis and subsequent infection Vague flank pain

2.

URETERIC STONES (even small stones can cause severe symptoms as the ureter is narrow) Ureteric colic pain (severe intermittent loin to groin pain ) Hematuria (gross or microscopic ) Irritative symptoms ( frequency, urgency) Signs of pyonephrosis ( upper urinary tract infection symptoms ) ; fever + chills + rigors, very ill due to sepsis

3.

BLADDER STONES May be asymptomatic Irritative symptoms ( frequency, urgency) Hematuria If infection present ( dysuria, fever ) INVESTIGATION

For diagnosis 1. KUB radiograph Radioopaque stone ( 90% of renal stones) False negative; too small, false positive; phlebolith (round with lucent centre),stools. Kidney; kidney size , stone Ureter ; trace the path of ureter, ureteric stones Bladder; bladder stones 2. Intravenous radiogram To visualize stone Can show dilated urinary system secondary to stone obstruction (hydroureter/hydronephrosis) 3. Ultrasound of kidney/ bladder Features of stones ; echogenic rim, posterior acoustic shadowing For complications 4. Urine test ( dipstick, UFEME, Urine c n s) -hematuria, pyuria 5. 6.

Intravenous urogram Dilated urinary system ( hydronehprosis, hydroureter ) MAG-3- renogram To give differential function of each kidney Normal ; 50% on each side, out of 100% of both kidney combined

PHYSICAL EXAMINATION GENERAL  signs of anaemia ( pale hand, conjunctiva)  very ill, in pain, cachecic, febrile, tachycardia ( in case of sepsis) SPECIFIC  no guarding, no rebound ( symptoms are out of proportion to sign)  tender suprapubic area ( in case of acute urinary retention )  positive renal punch (in case of pylonephritis)  kidney ballootable ( in case of hydronephrosis)

MANAGEMENT Conservative 1. Stone smaller than 5 mm should be treated conservatively (60% will passed out ); only treat if they do not pass after 4 to 6 weeks, or got symptoms 2. Treat UTI 3. Treat underlying disease eg; hypercalcemia 4. Diet -high fluid intake -low salt diet -restriction of red meat, dairy product, refined sugar -increase citrus fruit intake Surgical Indications :  S/S ; constant pain  complication  Obstruct urine flow  UTI  Significant bleeding  Kidney size increase 

unlikely to resolve with conservative treatment :  Does not pass after one month  Too large to pass spontaneously Types : 1. PCNL (percutaneous nephrolithotomy) – more than 20 mm (large stone ) 2. ESWL (extracorporeal shock wave lithotripsy) – 5 to 10 mm ( small stone) 3. Ureterorenoscopy with lithotripsy (URS + LL) – Stones along ureter 4. Cystolitholapaxy –bladder stone (for stone crushing) *renal stone 5 to 10 mm : Either ESWL OR PCNL *can refer ANDRE SURGICAL NOTES for more info

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1. 2. 3. 4.

What is the type of renal stones? How renal stones are classified ? Which stones are radioopaque, which stones are radiolucent ? Treatment modalities based on size,types, location of stones.. ( when to use PCNL, ESWL)

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Together in Delivering Excellence (T.I.D.E)

O&G Notes

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Together in Delivering Excellence (T.I.D.E) Pregnancy Induced Hypertension [Hamizah] HISTORY Risk factors: Primigravida, age>40, pregnancy interval>10 years, prior PE in a pregnancy by same partner,multiple pregnancy, Fly history of PE , obese, renal dz, DM, essential HPT, autoimmune dz (SLE,antiphospholipid syndrome) Clinical features -maternal manifestations: Presenting complaints: Weight gain & edema, headache, blurred vision, epigastric/ RUQ pain, SOB, oliguric, hemorrhagic manifestation, per vaginal bleeding (abruption) fetal mv (assess fetal well being) Complications: A. Maternal  Heart: high output, pulmonary edema  Placental abruption (d/t necrosis of distal end spiral arteries)  Hematology: thrombocytopenia  Renal: renal failure, nephrotic syndrome  Liver: subcapsular hemorrhage, infarction, rupture, congestion  Lung: aspiration pneumonia (during fits)  CNS: eclampsia, cerebral hemorrhage, retinal detachment B. Fetal  IUGR  Oligohydramnios

PHYSICAL EXAMINATION General examination  Vitals(BP, HR, RR, spo2)  Weight  Pallor, petechiae, edema Chest examination  (crepitations in pulmonary edema) Abdominal examination Epigastric or right upper quadrant tenderness Neurological examination Hyperreflexia, clonus Visual field testing Obs examination Symphysial fundal height (small for dates?) Palpate for fetal lie & presentation Palpate for uterine tenderness (woody hard indicate abruption) Estimated liquor volume DopTone for fetal heart sound

INVESTIGATION Maternal 1. FBC - Anemia(d/t hemolysis in HELLP) 2. Thrombocytopenia 3. Renal profile + serum uric acid 4. Raised serum creatinine & urea 5. Raised serum uric acid level in PE 6. 24 hr urinary total protein 7. Liver function test 8. Raised AST, ALT 9. Indirect hyperbilirubinemia 10. Coagulation profile 11. PT & APTT +/- d-dimers, fibrinogen (for DIVC) Fetal U/S  Estimated fetal weight, fetal lie & presentation, liquor volume, umbilical artery Doppler flow HELLP SYNDROME -Hemolysis (anemia) -Elevated liver enzyme (AST/ALT>70iu/L) -Low platelet (100mmHg (aim:90-100mmHg) 9. Dexamethasone if early delivery expected (0.3g/24 hr urine collection)

3) CHRONIC HYPERTENSION  

Presence of hypertension of at least 140/90 mmHg before 20th week of pregnancy or beyond 6 weeks postpartum. Includes essential & secondary hypertension.

4) CHRONIC HYPERTENSION WITH SUPERIMPOSED PRE-ECLAMPSIA    

Development of pre-eclampsia in patient with pre-existing hypertension Criteria used should include: worsening of hypertension proteinuria

5) ECLAMPSIA  

criteria for PE met presence of generalised tonic-clonic seizures which cnt be attributed to other causes



signs & symptoms of IE:

Headache, nausea & vomiting, visual disturbance, RUQ/ epigastric pain, frothy urine, pregressive edema at independent site

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Together in Delivering Excellence (T.I.D.E) MANAGEMENT OF ECLAMPSIA 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Call for help Left lateral position Secure airway, prevent pt injury Wait for convulsion to abate, if not iv diazepam 10mg bolus Max oxygenation-mask or intubation Catheterization for io chart Neurological examination Bishop score Prophylactic anticonvulsant therapy BP control Cervix favourable-vaginal delivery ; cervix unfavourable- c-sec

Anticonvulsive therapy MgSO4 à Maintainance dose: *IV infusion of 1g/hour * 5ml MgSO4 + 45ml 5%Dextrose sol. Infuse at 20ml/hour( syringe pump) OR * 10ml MgSO4 in 500ml D5% at 33 dpm (drips) Duration: – continue for 24hours after last fit or after delivery Monitoring for MgSO4 therapy: 1.Investigations  BUSE,FBC  Serum Ca2+,Mg  Renal function test (urea,uric acid,creatinine)  Coagulation profile  UFEME  ECG  GXM 2. STOP !!! If present signs of Mg toxicity: (a) RR < 16/min (b) Urine output < 25ml/hr (c) patellar reflex absent (d) Serum Mg > 3.5mmol/L (therapeutic range: 1.7-3.5) (e) BP < 90/60 mmHg 3. Antidote: Ca gluconate 10%-10ml Antihypertensive therapy initiatiate parenterally if BP> 160/110mmHg

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Together in Delivering Excellence (T.I.D.E) Placenta Praevia [Alliah] HISTORY Definition  Placenta that has implanted into lower segment of uterus after 28wks of gestation Risk factor  Multiple pregnancy  Multiparity  Previous C-sec/ERPOC/uterine surgery  Uterine structural abn. S&S

   

   

Assisted conception Advanced maternal age (>40) Previous episode Smoking

PHYSICAL EXAMINATION General   

Stable and less distress pt condition May appear pale BP,PR and pulse volume may fluctuate

Specific    

Soft and non-tender abdomen Fetal readily palpable Fetal not engaged,abnormal presentation and lie Usually normal fetal heart

Unprovoked painless PV bleeding Nature : fresh blood and intermittent Usually normal fetal movement Less distressed pt condition

Complications Maternal  Life-threatening haemorrhage-shock  Placenta accreta  PPH  Need of c-sec  Infection DDx

Fetal  Malpresentation  Fetal abn.  IUGR  Premature labor  Fetal hypoxia  Fetal death

 Placenta Abruptio  Vasa previa  Local causes

INVESTIGATION Laboratory FBC

Hb- to check for anemia TWBC & Platelet –to establish baseline * both Hb and platelet can be affected severely with massive blood loss (anemia and DIC)

GXM Coagulation profile (when indicated) Renal profile Imaging 1) Transabdominal & Transvaginal U/S  To locate placenta  To confirm diagnosis  TVS : esp. when locating posterior PP that obscured by overlying fetus & more accurate 2) Color Doppler U/S  To diagnose in pt high risk of placenta accreta (previous c-sec)

MANAGEMENT Conservative  Pt with minor and major (no previous bleeding) PP Consider : - Distant house-hospital - Transportation - Educational level & know how to take care herself Educate : - Rest and no heavy work - Avoid SI - Avoid abdominal massage - Immediate come to hosp. If presence of contraction pain * Pt with major PP (had previous bleeding) : should admit from 34weeks Acute Resuscitation (RAINBOVV) +  V/S monitoring hourly  Pad chart monitoring  Assess baby : CTG and US  Give IM Dexamethasone if < 34wks  Check maternal rhesus status Caesarean Section Emergency  Gestational age > 36 wks of gestation  Irrespective of gestational age if : profuse bleeding &/or fetal distress Elective  At 38 or 39 wks  If : a) placenta edge 1cm) * Minor PP – SVD if placenta minimum 2cm away from cervical os

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Together in Delivering Excellence (T.I.D.E) 1.

Classification UK Type I. Lateral : < 5cm from os II. Marginal : edge at int.os  Anterior  Posterior III. Assymetrical cover os IV. Symmetrical cover os @ anterior & posterior

Minor

Major

US Complete : covering os Partial : partially cover os Marginal : edge within 2 cm from int.os Low-lying : edge within 25cm from int.os

2.

How can you diagnosed placenta accreta?  Color Doppler U/S (whether there is blood flow to the bladder)  MRI  Grey scale U/S

3.

When we opt for McAfee Regime?  Bleeding is not life-threatening & baby is still premature [expectant mx]  Components : a) Admit pt to the ward b) Close observation for any further bleeding c) Availability of atleast 2 units of gxm d) Availability of the ot

4.

If now pt is 38 weeks & pt admitted for elective LSCS. How do u prepare this patient?  Consent (operation, blood transfusion & explain future risk of Csec and the need for Csec the next pregnancy, risk for hysterectomy)  FBC - check for Hb (aim at least 11g/dl)  GXM 4 pints  CBD should be done in OT

5.

Mode of anaesthesia in this patient? GA  Not spinal because spinal can cause hypotension  In PP surgery, there will be lots of blood loss & patient can go further hypotensive  GA - is easy to control the circulation in case the surgery went complicated

85

Together in Delivering Excellence (T.I.D.E) PPROM (Preterm Pre-Labour Rupture Of Membrane) [Baisyatul] HISTORY 1.

2.

3.

Presenting complain Sudden gush of warm fluid vaginally, usually followed by continuous dribble, colourless fluid Volume ( soaked sarong/ pad) Must distinguish from leaking urine ( ask about frequency, urgency, dysuria) as incontinence or ITI may present in similar way Smell ( urine smell, foul smelly, odourless) Vaginal discharge- UTI Per-vaginal bleed-( a/w abruption) Uterine irritability or contractions Fetal movement may reduce, frequency or strength also reduced Risk factor assessment Prev history of preterm labour/PPROM Twin pregnancy Polyhydramnions Uterine/cervical abnormalities (fibroids) Recurrent antepartum haemorrhage Infection ( fever, vaginal discharge) Smoking Cocaine abuse Low BMI mother Asses complication Chorioamnionitis ( maternal pyrexia, vaginal discharge, uterine tenderness )

1.

PHYSICAL EXAMINATION General examination: Signs of infection: tachycardia, high temperature, flushed appearance

2.

Abdominal examination: Uterus smaller than date due to oligohydramnions Malpresentation (beware cord prolapse) Uterine tenderness if chorioamnionitis present

3.

Sterile speculum examination (definitive diagnostic tool) Preferably after patient has been resting supine for 20-30 minutes A pool of amniotic fluid in posterior fornix Visualize the cervix; fluid may be seen trickling through the external os and dilatation of cervix can be assessed

Digital vaginal examination should be avoided: Can stimulate prostaglandin production Introduce organism into cervical canal

INVESTIGATION Maternal Check pool of liquor by: a) Litmus paper (red to blue) b) Nitrazine test (turn to black) c) Ferning test (microscopic examination to look for fetal epithelial cells) Full blood count: check WBC, CRP for early marker for infection High vaginal swab: culture for gonorrhoea, Chlamydia, trachomatis Low vaginal swab: GBS Urine FEME: to rule out UTI

1. 2.

Fetal Serial CTG (beware of increasing baseline heart rate or fetal tachycardia early sign for intrauterine infection Ultrasound: look for AFI, fetal biophysical profile Fetal fibronectin is a useful confirmatory test if doubt about diagnosis

5.

3. 4.

6. 7.

8.

MANAGEMENT Admit patient (inpatient management) Monitor patient (Vigilance for chorioamnionitis) Clinical (Maternal fever, tachycardia, uterine pain/tenderness, purulent vaginal discharge, fetal tachycardia) Laboratory investigations e.g. total white count and differential count, C-reactive protein, HVS C&S Biophysical profile of fetus IM dexamethasone nd 12mg stat, repeat 2 dose after 12 hour Prophylaxis antibiotic Erythromycin 250mg orally 6hourly for 10 days To reduce risk of chorioamnionitis If chorioamnionitis: cephalosporin + metronidazole (augmentin) immediately Discharged after observe 48-72 hous if no more leaking liquor, no infection, no labor symptoms Delivery indicated if: Chorioamnionitis is diagnosed Fetal distress occurs Post-natal: Maintain vigilance and screening for infection. Neonatal screen for sepsis

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Together in Delivering Excellence (T.I.D.E) COMMON QUESTIONS 1. Complications Maternal complication: 1) Infection - Associated with 30% subclinical chorioamnionitis with PPROM. 2) Abruptio placenta is evident in 4-7% of women with PPROM. 3) Psychosocial sequelae, particularly related to PPROM, with the disruption created by maternal hospitalisation and continued observation associated with uncertain fetal/neonatal prognosis. 4) Increased likehood of operative delivery associated with induction of labour will increased the chance of maternal complications. 5) Increased incidence of marginal cord insertion and Battledore placenta which may account for increased incidence of retained placenta. This in turn may be associated with the known increase in the incidence of primary and secondary post-partum hemorrhage. 6) Associated with 10% incidence of endomyometritis Fetal complication: 1) Prematurity and risks of prematurity like RDS, NEC, intraventricular hemorrhage, etc. 2) Neonatal sepsis - 2-4% 3) Oligohydroamnios tetrad characterised by facial anomalies, limb position defects, pulmonary hypoplasia and impaired growth, all of which will lead to neonatal morbidity. 4) Fetal hypoxia due to greater risks of cord prolapse, cord compression and abruptio placenta 5) Neonatal morbidity will be increased due to mechanical difficulties encountered with delivery either by vaginal or abdominal route as a result of increased incidence of malpresentations and reduced volume of amniotic fluid 2. Advise upon discharge - No sexual intercourse - Come back if leak again, contraction pain, infection - Frequently follow up antenatally 3. Role of tocolytic in PPROM - No significant benefit in prolongation of pregnancy to term - Allow course of steroid for fetal lung maturation to be completed - To facilitate transfer of undelivered mother to a unit that able to provide appropriate neonatal care Reference: 1. Obstetric 10 Teachers 19th edition (MOST) 2. Specialist notes 3. Student notes o&g

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Together in Delivering Excellence (T.I.D.E) Heart Disease (HD) in pregnancy [Hidayah]

HISTORY  Epidemiology : 1 % of pregnancy  Risk factors : 1. CHD 2.hypercholesterolemia 3. Family hx of HD , hypercholesterolemia 4.hx of RHD during childhood  History 1. Diagnosis -type of lesion, when/where/how?, causes (CRHD,CHD,HPT), procedure( exercise test,echo), surgical/corrective done?, any improvement/residual? Medication& diet, compliance/f.up, cx, admitted before? 2. Symptom – fatigue at rest, exertional chest pain, orthopnea, PND, palpitation, exertional syncope, NYHA classification* 3. Any pre conceptional advice – surgical advice?, explain about mother& fetal risk, willing for frequent f.up&long stay in ward, should have early booking. 4. Booking- when, ix,echo&result, early u/s for dating (risk of prematurity), u/s for CHD~20W 5. Symptom that may aggravated heart failureAnemia (pallor, lethargic), UTI (dysuria, frequency), URTI (running nose, sorethroat) 6. Pregnancy- in labour ? fetal movement

PHYSICAL EXAMINATION General o Anemia o Clubbing, infective endocarditis signs, o xanthoma o Pulses (arrhythmias) o Blood pressure o Jugular venous pressure o Cyanosis o Dental carries o ankle edema Abdomen examination (as usual)  Uterus smaller than date or any abnormalities Chest examination  Shifted apex beat  Murmur  Basal crepitation

INVESTIGATION Maternal 1. 2. 3. 4. Fetal

FBC – Hb , WBC ( can aggrevate HF) Urine FEME (TRO UTI) ECG Echocardiogram

1. CTG : to look evidence of fetal hypoxia 2. U/S : detailed detection of fetal anomalies, AFI, fetal growth&placentation.

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Together in Delivering Excellence (T.I.D.E) MANAGEMENT Preconception 1. Fully accessed 2. Treat aggresively any medical illness (try to stabilize before pregnancy) 3. If surgery needed, do b4 pregnancy (mitral valve replacement in MS) 4. Counselling about: Effect of haemodynamic changes&maternal risk Effect of fetal growth & preterm Genetic transmission Effect of maternal drug & compliance Need for frequent admission & long stay 5. Encourage complete family earlier&discourage from multiple pregnancy.

 Time and mode of delivery 1. Mild & moderate heart dis Aim for spontaneous vaginal delivery Avoid induction of labour if possible 2. Admit patient early, wait for birth if : Severe heart disease Develop acute heart failure 3. Prepare for preterm labour for severe heart dis pt (high chance to deliver at 32-34W in severe MS) 

Intrapartum 1. Aim delivery within 6 H 2. Stop heparin b4 pregnancy (clexane stop 6H b4 delivery) 3. Prop up to left lateral tilt 4. Continue ECG, CTG & pulse oximeter 5. Give oxygen (3L/min) 6. Give epidural anaestesia 7. AB prophylaxis (in severe cases) IV ampicillin 2g stat & 8 H later 2x doses IV gentamicin 800mg & 8H later 2x dose 8. Avoid fluid overload by close monitoring during fluid therapy nd 9. Shortened 2 stage by using instrumental delivery rd 10. For 3 stage, give syntocinon(don’t give ergometrine)



Postpartum 1. Keep pt in labour room for 6-24H after delivery 2. Give Lasix 40mg stat (to prevent fluid overload during ntrapartum) 3. Admit ward at least 1 w 4. Close monitoring (i/o chart, BP, PR, RR, ECG) 5. Look for any complication 6. Continue prophylaxis AB for 5 days 7. Advise for contraception (POP,barriermethods, sterilizationBTL)



Management of Heart Failure 1. Inform cardiologist,obstetrics,anes-send to CCU/ICU 2. Semi-recumbent (propup) 3. Oxygen 4. Morphine (pain relief&dilate vein) 5. Frusemide 6. Digoxin-dysrhytmia 7. Endotracheal intubation 8. Assisted aspiration 9. Cardiac surgery 10. Leg exercise/stocking (prevent DVT)

Antenatal  Booking 1. All mother examined carefully for CVS abn. 2. If suspected, refer to cardiologist & do echo 3. Known case should book early 4. Cases should be managed in combined clinic 

Antenatal 1. Regular antenatal checkup  Assess maternal : ( sx HF and NYHA), ECG, vital sign  Assess fetal : detailed scan for congenital anomalies, serial growth scan to detect IUGR, Fetal kick chart, CTG. 2. Avoid factor aggravate HF and treat Anemia Infection- UTI, URTI Hyperthyroidism Arrhytmia Multiple gestation 3. Advise about : rest, no smoking, compliance to hematinic, care about infection, dental checkup (prevent I.E) 4. Anticoagulant indicated in pt congenital heart disease who have pulmonary HPT or artificial valve replacement. 3 types of regime :  Continue warfarin throughout pregnancy, replace heparin for delivery (1-2w prior to delivery st  Replace warfarin with heparin in 1 trimester,other same st as 1 regime  Use heparin throughout pregnancy

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1.

CVS Normal physiology in pregnancy a.

b. c. d. e. f. g.

2.

Risk stratification - maternal risk Low risk (mortality 3.8kg) o IUGR (10g/dL hb prior to delivery Intra:  GSH rd  PPH prevention – active management during 3 stage  Start transfusion if severe anemia or excessive blood loss Post:  Iron supplement  Counselling regarding contraception and spacing Admission:  When need for transfusion (moderate, >37weeks with sign of labour or severe or with complication)  When have active blood loss

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Together in Delivering Excellence (T.I.D.E) 1. Hb level (expected to be lower than normal in pregnant lady): Anemia @booking 5mm provides excellent in size, particularly in images of deep tissue, eg: myometrium, rectovaginal septum endometrium & areas of adenomyosis Laparoscopy Dx only confirmed - gold standard by histology after - typical endometrial hysterectomy appearance “powder burn” – small brown/ black puckered lesion look like remaining cigarette burn

 hypoechoic, but can be sooechoic or even hyper compared to N myometrium  calcification is seen as echogenic foci with shadowing  cystic areas of necrosis or degeneration

Hysterosalpingograp hy/ hysteroscopy - detect submucous fibroid

General  Anemic – pallor, conjunctiva pale  Lethargy Specific Endometriosis  Palpable mass  Tender – if rebound tenderness + rigid abdomen indicate of large endometrioma ruptures, spilling blood into peritoneal cavity (acute abdominal pain)  Pelvic exam – areas of tenderness / palpabe mass d/t adhesions or endometrioma.  Rectovaginal exam – tender nodular indurations along the uterosacral ligaments Adenomyosis  Pelvic exam: - Symmetrical enlarged uterus & tender all over - Soft and boggy uterus Fibroid    

Uterus palpable if > 14w Usually non tender, if present only occur over one localized fibroid (d/t degeneration) Firm in consistency & well defined margin Pelvic exam : - Enlarged uterus - regular/ irregular - uterus not felt separate from the swelling - cervix move with movement of swelling - move side to side

MANAGEMENT Adenomyosis:  definitive tx is hysterectomy with or without ovarian conservation Endometriosis Medical 1. Analgesic : NSAIDs 2. Combined oral contraceptive (COC) – taken continuously for 6m – induce amenorrhea 3. Progestogens – if COC is at risk 4. Gonadotropin releasing hormone (GnRH) agonist – relieve severity of sx by induce state of hypogonadotropic hypogonadism/ pseudomenopause with low circulating estrogen Surgical 1. Laparoscopic with diathermy, laser vaporization or excision – drained & inner cyst lining should be excised 2. Hysterectomy & bil salpingooophorectomy (definitive)  for severe/ progressive dz  women whose completed families followed by HRT

Fibroid Conservative Asymptomatic & detected incidentally  repeat clinical exam/ us after 612month interval Medical 1. Gonadotropin releasing hormone (GnRH) agonist – shrinking fibroids by downregulate the pituitary thus reduce estrogen level. Limited to use in preparation for surgery (myomectomy or hysterectomy) Surgical 1. Hysteroscopic removal – menorrhagia a/w submucous fibroid or fibroid polyp 2. Myomectomy  bulky fibroid that causes pressure sx  preservation of fertility 3. Hysterectomy (definitive) 4. Uterine artery embolization (UAE) – embolization of both uterine arteries under radiological guidance. Lead to shrinkage of fibroid & reduction in menstrual blood loss

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Together in Delivering Excellence (T.I.D.E)

Types of fibroid Submucous fibroid – whorled tumour located adjacent to & bulging into the endometrial cavity Intramural fibroid – centrally within myometrium Subserosal fibroid – at the outer border of the myometrium Pedunculated fibroid – attached to the uterus by a narrow pedicle containing blood vessels

Different types of degeneration in fibroid?     

Red Hyaline Cystic Calcification Malignant/sarcomatous

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Together in Delivering Excellence (T.I.D.E) Miscarriage [IQbaL] HISTORY Definition : Spontaneous loss of pregnancy at or before 24 weeks gestation 10-20% incidence in confirmed pregnancy Majority at 1st trimester Risk factors (RF) a) Embryonic  Chromosomal abnormalities b) Maternal  Advanced maternal age (>35yo, dec good no. of good Oocytes)  Genital tract infection (bacterial vaginosis)  Medical/endocrine disorder  Uterine abnormalities  Drugs/chemicals

INVESTIGATION 1. 2. 3. 4. 5.

UPT FBC – infection (anemia, TRO septic miscarriage) Rhesus blood group Serum B-hCG titre – to confirmed pregnancy Tran-vaginal US  Key Dx of miscarriage provided serum B-hCG >1500UI/L i. empty gestational sac ii. no visible yolk sac iii. crown-rump length > 7mm but no fetal heart activity  Help to differentiate btw complete/incomplete

Key diagnostic factors

i. ii.

Presence of RF

Vaginal bleeding with or without clots Other diagnostic factors  Suprapubic pain, low back pain  Recent post-coital bleed



Uterine structural abnormality

Chronological History Confirmed pregnant? UPT done? Hx post-coital? Any atypical blood clot expelled? Severity of vaginal bleeding? – flooding, clots, inc in duration & no. of pads used per day, anemic sx Important TRO ectopic pregnancy (pelvic/suprapubic pain a/w fainting attack or unexplained anaemia) Recent genital infection? Fever? Hx of recent trauma

PHYSICAL EXAMINATION GENERAL  Clinically well  If ill-looking – significant blood loss SPECIFIC A. CVS  Any pale, tachycardia, hypotension (anemic)  Dyspnea (ectopic pregnancy) B.

Abdominal-pelvic  Size of uterus

C.

Perineum  Any local lesion that lead to bleeding

Speculum examination  Early pregnancy tissue?  Cervical Os : open/closed?  Laceration, cervical ectropion?

MANAGEMENT Initial Management  Monitoring : BP, pulse rate, temperature  Lab Ix : Hb level, GXM ( if pt is severely compromised)  Pt with miscarriage can have expectant, medical or surgical management Expectant No intervention May have unplanned surgery if bleed heavily Surgical ERCP (evacuation of product of conception) Successful rate : 95-100% Risk of cervical trauma, subsequent cervical incompetence, uterine perforation, intrauterine adhesion & post-operative pelvic infection Medication Prostaglandin : Orally (misoprostol) or vaginally (Gemeprost) Increase rate of successful : prostaglandin + Mifepristone (progesterone agonist) Counselling To ensure pt understand most miscarriage are nonrecurrent

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Together in Delivering Excellence (T.I.D.E) WHO classification Type

THREATENED [cervical os CLOSE]

Clinical Presentation

U/S finding

Management i. ii. iii. iv.

 Unprovoked vaginal bleed  With/out lower abd pain  Occur 20mm) but no fetal pole identified

REASSURE pt Admit if excessive bleeding TCA scan in 1-2 weeks Advice : proper rest at home, no strenuous or heavy work, no SI until 12th week gestation & no further bleed Give Duphaston : to restore luteal f(x) & relax smooth ms of uterus Anti-D immunoglobulin if indicated Stabilized pt Manual evacuation : digitally or with sterile ovum or sponge-holding forceps Analgesic Counselling Anti-D immunoglobulin if indicated

ii. iii. iv. v.

Controlled bleeding (IV/IM Ergometrine or IM syntometrine) Surgical evacuation (D&C) Analgesic Counselling Anti-D immunoglobulin if indicated

i. ii. iii.

Analgesic Counseling Anti-D immunoglobulin if indicated

i.

ii.

Cervical softening (vaginal gemeprost 1mg, oral/vaginal misoprostol) 2-3 hour before evacuation Surgical evacuation under GA/reginal anaesthesia

Complication Septic miscarriage : ascending bacterialinfection secondary to incomplete miscarriage or termination of pregnancy  Common organism : E.coli, bacteroids, streptococci  Symptoms : unwell, fever, lower abd pain. Foul smelling vaginal discharge  Signs : spiking temperature, lower/pelvic pain, guarding  U/S : presence of POC  Management o Admit pt o Ix : FBC, Blood C&S, swab from endocervix fot C&S, BUSE and creat & LFT o Fluid resuscitation o Anti-biotic (cover gram positive, negative & anaerobes DIFFERENTIAL DIAGNOSIS CONDITION Differentiating signs/symptoms Differentiating test  TAS is diagnostic : no intrauterine gestational sac, complex or cystic adnexal mass with/out free fluid in pouch of Douglas  Atypical symptoms that can be missed ( iliac fossa/suprapubic pain, unexplained pallor, tachycardia or syncope  Serial serum B-hCG + single measure of Ectopic pregnancy progesterone : to distinguish between early viable,  O/E : adnexal tenderness or suggestion of haemoperitoneum poor prognosis or ectopic gestation  If in doubt, laparoscopy to confirm Dx : distended, ruptured or haemorrhagic fallopian tube or other extra-uterine preg site.  Uterine size more larger than expected gestational age  TAS : classic Snow-storm appearance Hydatidiform mole ( Molar )  Pregnancy Sx are marked  Partial hydatidiform : reveal fetus but unusuallooking placenta  Very rare : passed some molar, grape-like tissue  Suprapubicpain + DYSURIA & FEVER  Urine microscopy and culture Cystitis  May have haematuria Pregnancy co-excisting with a  May be suspected from appearances of the ecto-cervix on  Confirm after U/S or by spontaneous avulsion of bleeding cervical polyp/ large speculum examination polyp ectropion

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Together in Delivering Excellence (T.I.D.E)

ORTHOPAEDIC

Notes

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Together in Delivering Excellence (T.I.D.E) Osteomyelitis [Fatin] HISTORY *Inflammation of bone caused by infection o Epidemiology :  cause by Staph A. (H.influenza in children)  site : children (metaphysis and epiphysis of long bone) & adult (spine, pelvic & foot if has DFU) o Causes :  Hemato spread – UTI, pneumonia  Local infection – infected puncture wound  Direct contamination – open #, iatrogenic (surgry) o Risk factor :  DM, Sickle cell dz, peripheral vascular dz, chronic dz, alcohol, steroid Rx recent injury, ortho surgery o S&S :  Pain, malaise, fever  Swelling, redness, tender, warmth, ↓ROM o Complication :  Spread-septic arthritis (joint), metastatic OM (other bone)  Shortening / deformity (physis is damage)  Chronic OM –pain, fever, redness, swelling, discharge sinus  No- union fracture

PHYSICAL EXAMINATION General  Ill looking, in pain  Vital sign : fever, tachycardia  Sign of septicemia Specific  Swelling, redness, tender, warmth, ↓ ROM  Chronic – discharge, sinus, non-heal ulcer ∆∆ 1. 2. 3. 4.

INVESTIGATION o

Laboratory  FBC- leukocytosis  ESR - ↑  Blood culture  Needle aspiration

MANAGEMENT o

o o

Imaging  X-ray - Acute : First 10 days –normal finding Later – periosteal rxn, lytic area, soft tissue swelling - Subacute (Brodie’s abcess) : lytic area surrounded by sclerotic bone - chronic : sequestrum, involucrum, cloaca, sinus tract  Bone scan – positive b4 x-ray changes appear

Abscess Malignant bone tumour (Osteosarcoma, Ewing sarcoma Lymphoma 4) Metastatic bone tumour

Non-surgical  Antibiotic (3-6/52)  Adult : cloxacillin & fusidic acid rd  Children : 3 gen cephalosporin (gram –ve)  Analgesic Surgical  Drainage of abcess  Debridement of infected, dead bone  Bone graft/ packing material  Removal of implant

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1.

List the factors that predispose to post-traumatic infection. a) Inadequate debridement. b) Early closure of the wound. c) Unfixed / unstable fracture. d) Wound tension. e) Tight dressing. f) Haematoma formation. g) Use of foreign material implant eg. Internal fixation.

2. What are the complication of osteomyelitis? I. General :  Septicaemia  Metastatic abcsess ii. Local :  Septic arthritis  Spontaneous fracture  Shortening/ Deformity  Chronic osteomyelitis. 3.

Why metaphysis is affected in children  Highly vascular  Thin cortex  Hairpin like arrangement of capillary – blood stasis  Lack of pmn

4.

Pathogenesis

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Together in Delivering Excellence (T.I.D.E) Fracture – Malunion & Non Union [Rozana] HISTORY 

Non union = bone/fracture fails to unite within expected time, with the evidence of cessation of fracture healing.



Malunion = The partial and incorrectly angled joining of two or more large fracture fragments



Risk factor/causes :  Malunion : Failure to reduce a fracture adequately, Failure to hold reduction while healing proceeds, Gradual collapse of comminuted or osteoporotic bone.  Non union : Inadequate blood supply, Infection, Inadequate fracture immobilisation , Intact fellow bone, interposition, Smoking, NSAID



Specific :  Malunion : tenderness, deformity & shortening of the limb, surgical scars , swelling , Limitation of movements, 

Non union : painless, deformity

Sx :  Malunion : pain, loss of function, deformity, swelling, crepitus, abnormal movement, or positioning of a limb, soft tissues  Non union : painless, deformity INVESTIGATION

I.

PHYSICAL EXAMINATION

Imaging :  Non union : a) Atrophic non-union : - Bone looks inactive / cessation of fracture healing (Bone ends are often tapered / rounded), Relatively avascular b) Hypertrophic non-union : - bone gap, Excessive bone formation on the side of the gap, (callus) 

Malunion : Present of fracture line , altered anatomical position

MANAGEMENT i. Non union mx  Depends on the factors : Infection, Inadequate blood supply, Inadequate immobilisation  Mx aimed at optimizing 1)biology (infection, blood supply, bone graft), 2) mechanics (skeletal stabilization)  Atrophy – Fixation & bone grafting  Hypertrophy – Rigid fixation ii. Malunion  Angulation in a long bone (> 15 degrees) & Marked rotational deformity → Osteotomy & internal fixation +/- bone graft  Shortening (> 3cm) in 1 of the lower limbs → A raised boot OR Bone operation

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer Notes [any classification,staging, mnemonic etc] 



Indication for ORIF a. Failed conservative rx b. 2# in 1 limb c. Bilateral identical # d. Intraarticular # e. Open # Emergency mx for open #  7 ‘As’ o ATLS  Correct shock , give blood >1.5 L lost or continued bleeding, control of bleeding may require surgery o Assesment  Neurovascular status, soft tissues and photograph wound (reduces number of wound inspection) o Antisepsis  Take swab form wound  Use copious irrigarion with sterile 0.9% saline  Cover with a large antiseptic soaked dressing o Alignment  Align # and splint (+ pain relief) o Anti tetanus

o o 

Cx

    









 Check status and immunize appropriately Antibiotics rd  3 gen cephalosporin eg. Ceftriaxone 1g/24h +/- IV mtronidazole if grossly contaminated Analgesia  Intravenous opiate analgesia titrated to effect

Immediate Internal bleeding External bleeding Organ injury Nerve/ skin injury Vessel injury (limb ischaemia)

   

Later – local Skin necrosis/ gangrene Pressure sores Infection Non/ delayed union

   

Later – general Venous/ fat embolism PE Pneumonia Renal stones

Gustillo classification of open # o Type I - low energy wounds 1cm, causing moderate tissue damage o Type III – all high energy injuries irrespective of wound size  IIIA – adequate local soft tissue coverage  IIIB - inadequate local soft tissue coverage  IIIC – implies arterial injury needing repair Methods of traction (hold the reduction) o Skin traction – uses adehesive strapping to attach the load, cons : load cannot be great & sensitivity to adhesive o Fixed - Thomas splint, weight can be added over a pulley to relieve pressure on ischial tuberosity o Skeletal traction – pin thru bone, bigger forces can be employed o Balanced – weight of limb against the load, enable pt to easily lift leg off bed o Gallow’s – suitable for children up to 2 years, buttock rise above the head FES o Clinical condition in which circulating fat emboli/macroglobules lead to multisystem dysfunction o Common in long bone fracture and pelvic fracture, more frequent in closed fracture than open fracture. o Usually asymptomatic, few patient develop S&S of multiorgan dysfunction ( triad of brain, skin, lungs) o Source of fat emboli – bone marrow o Management is supportive, with an estimated mortality rate of 5 -15 % site of bone graft taken? o

ilium and the fibula are the most common sites for bone-graft harvesting

Radiographic Determinants of Healing: - restoration of cortical continuity (look for healing on 4 cortices - AP and lateral views); - loss of distinct fracture line; - presence of callus (w/ IM nail or external fixator)

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Together in Delivering Excellence (T.I.D.E) Gouty Arthritis [Farhan ] HISTORY  Monoarticular pain with edema and inflammation  >50% occurs at MTP of big toe (podagra)  Other joints are ankle, foot, small joints of hands, wrist, elbow and knee  Can be polyarticular (10%)  Male predominance (4:1)  Caused by deposition of monosodiumurate crystals in/near joints  Precipitated by e.g. trauma, surgery, starvation, infection or diuretics (thiazide)  Acute vs chronic attack  Causes (primary vs secondary): i. Hereditary ii. High purine diet iii. Alcohol excess iv. Diuretics v. Leukaemia vi. Cytotoxics (tumour lysis)  Comorbidities: i. Cardiovascular disease ii. Hypertension iii. Diabetes mellitus iv. Chronic renal failure  Complications: i. Severe degenerative arthritis ii. Secondary infections iii. Urate nephropathy iv. Renal stones v. Fractures (in joints with tophi) INVESTIGATION

PHYSICAL EXAMINATION Acute:  Pyrexia often present  Red, warm, tender and painful joint(s)  Usually monoarticular  Most common MTP joints Chronic:  Tophi (chalky coloured nodules on pinna, tendons, joints) Chronic arthritis (secondary OA, restriction of joint movements) MANAGEMENT Asymptomatic hyperuricaemia should not be treated 1. Treat acute attacks  Use high-dose NSAIDs or coxib  If contraindicated; use colchicine  Steroids can be used  Rest and elevate joints  Ice packs may help

2. Prophylaxis for acute flares  Allopurinol 100mg/24hr, increasing every 2 weeks (max 900mg/24hr) o SE: rash, fever, WCC low o Can trigger acute attack, so wait until 3 weeks after acute attack and cover with NSAIDs or colchicine 1. Serum urate – high level not diagnostic, low level does not o Excreted through kidney (beware in renal exclude diagnosis impairment) 2. 3. 4. 5.

WBC – often raised ESR – often raised Synovial fluid analysis – Negative birefringent (under polarized light), needle shaped crystals X-rays – soft tissue swelling, punched-out erosions (difference from RA: maintenance of joint space, does not involve joint capsule, absence of periarticular osteopenia)

 Febuxostat (80mg/24hr) o Alternative if allopurinol is contraindicated or not tolerated o SE: increase LFT o Metabolised and excreted by liver 3. Diet (low purine, hydration) and exercise

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Together in Delivering Excellence (T.I.D.E) Differential diagnosis

Differentiating signs

Pseudogout  Presentation may be identical to that of gout  Is less common in young age (0.9  >0.5-Ulcer healing  1 hour for > 6 weeks E : erosion on xray S : symmetrical arthritis > 6 weeks 4.

Detailed history about risk factor OA (mainly affect cartilage) Age Older age >45 y.o Family hx

-

Sex

Equal Men < 55 y.o Women >later in life Non-immune -age,genetic,previous injury to joint,obesity,hormone

Trigger

RA (mainly affect synovium) At any age even in children Average : 30- 50 y.o More in RA Women > men 3:1

Autoimmune -genetic,infection,hormone,smoking

bilaterally,symmetrical,destructive and performing polyarthropathy.

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Together in Delivering Excellence (T.I.D.E) PERSONAL NOTES

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